الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
Immune thrombocytopenic purpura is an acquired organ-specific autoimmune thrombocytopenic syndrome characterized by immune-mediated platelet destruction due to binding of immunoglobulin G autoantibodies against GpIIb/IIIa or GPIb/IX platelet glycoproteins. It is usually a benign, self-limiting disease in children Patients with immune thrombocytopenic purpura possess activated platelet autoreactive B and T cells and cytokine imbalance, suggesting loss of peripheral tolerance in immune thrombocytopenic purpura patients. T-helper cells and the cytokine they produce play a key role in immune thrombocytopenic purpura. Cytotoxic T-lymphocytes can also induce the lysis of autologous plateletsThe immune response to glycoproteins in immune thrombocytopenic purpura is usually modulated by CD4+ effector cells and CD8+ cytotoxic cells. In the thymus, T cells lose either the CD4 or CD8 antigens and are released as either CD4+ effector or CD8+ cytotoxic T cells. Some self-reactive T cells survive thymic depletion, and persist in peripheral blood as autoreactive and mediate autoimmunityThe current study was a case control study conducted at Department of Clinical Pathology in Assiut University Hospital. It was conducted in the period between 30th July 2020 and 1st July 2022. the study aimed to the role of interleukin-37 in the pathogenesis of immune thrombocytopenic purpura. In addition to, study the relation between T- lymphocyte, natural killer cells and interleukin-37 levels in immune thrombocytopenic purpura patients.